Open AccessTranscriptional Inhibition of Protease-Activated Receptor-1 Expression by Prostacyclin in Human Vascular Smooth Muscle Cells
Author(s) -
R. De Pape,
Bernhard Rauch,
A Rosenkranz,
Gernot Kaber,
Karsten Schrör
Publication year - 2007
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.107.159483
Subject(s) - forskolin , adenylyl cyclase , vascular smooth muscle , prostacyclin , iloprost , activator (genetics) , phosphodiesterase 3 , endocrinology , rhoa , receptor , thrombin , medicine , downregulation and upregulation , agonist , phosphodiesterase , protein kinase a , biology , camp dependent pathway , phosphodiesterase inhibitor , signal transduction , microbiology and biotechnology , stimulation , kinase , platelet , biochemistry , enzyme , smooth muscle , gene
Stimulation of protease-activated receptor-1 (PAR-1) by thrombin causes vascular smooth muscle cell (SMC) mitogenesis and has been implicated in the vascular response to injury. Vascular injury is also associated with enhanced formation of PGE2 and PGI2 (prostacyclin). This study investigates whether PGI2 and PGE2 modify the expression of PAR-1 and the cellular response to thrombin in human SMC.
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